Complete dissociation of DOCA-salt hypertension and red cell ion transport alterations
Jazyk angličtina Země Nizozemsko Médium print
Typ dokumentu časopisecké články, práce podpořená grantem
PubMed
1447948
DOI
10.1016/0024-3205(92)90044-p
PII: 0024-3205(92)90044-P
Knihovny.cz E-zdroje
- MeSH
- deoxykortikosteron MeSH
- desmopresin aplikace a dávkování MeSH
- draslík metabolismus MeSH
- erytrocyty metabolismus MeSH
- iontový transport MeSH
- krevní tlak MeSH
- krysa rodu Rattus MeSH
- osmolární koncentrace MeSH
- potkani Brattleboro MeSH
- renovaskulární hypertenze metabolismus MeSH
- sodík metabolismus MeSH
- tělesná hmotnost MeSH
- vasopresiny nedostatek MeSH
- zvířata MeSH
- Check Tag
- krysa rodu Rattus MeSH
- ženské pohlaví MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- Názvy látek
- deoxykortikosteron MeSH
- desmopresin MeSH
- draslík MeSH
- sodík MeSH
- vasopresiny MeSH
Our previous study revealed major ion transport alterations that resulted in a pronounced elevation of red cell Na+ content in DOCA-salt treated homozygous vasopressin-deficient (DI) Brattleboro rats in which only a moderate increase of systolic blood pressure occurred. In contrast, no changes of red cell Na+ content were observed in heterozygous vasopressin-secreting (non-DI) Brattleboro rats with a severe DOCA-salt hypertension. Using a chronic supplementation of DI rats with an antidiuretic agonist dDAVP (1-desamino-8-D-arginine vasopressin) we did not demonstrate any significant changes of red cell ion transport in dDAVP-treated DI rats with a fully developed DOCA-salt hypertension. The absence of ion transport alterations seems to be mainly due to dDAVP-induced correction of altered K+ metabolism seen in DOCA-salt treated DI animals. It can be concluded that DOCA-salt hypertension can develop even without red cell ion transport alterations which are usually caused by cell K+ depletion.
Citace poskytuje Crossref.org
Research on Experimental Hypertension in Prague (1966-2009)
